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Department of Biomedical Engineering and Department of Pharmacology and Physiology, University of Rochester, Rochester, NY 14642, USA
We addressed the role of endothelial cells (ECs) in metabolic dilatation of skeletal muscle arterioles in anaesthetized mice in situ. Electrical field stimulation was used to contract the cremaster muscle for 15 s at 30 Hz. Diameter was observed using bright field microscopy. In controls, muscle contraction produced a 15.7 ± 1.5 µm dilatation from a baseline of 17.4 ± 1.6 µm. Endothelial denudation (-EC) via intraluminal perfusion of air abolished this response (1.6 ± 1.2 µm in -EC, P < 0.05), identifying endothelium as the primary vascular cell type initiating the dilatation. To investigate the role of EC Ca2+ in metabolic dilatation, arteriolar ECs were loaded with Fluo-4 AM or BAPTA AM by intraluminal perfusion, after which blood flow was re-established. Ca2+ activity of individual ECs was monitored as a function of change from baseline fluorescence using confocal microscopy. In ECs, whole cell Ca2+ increased (>10%, P < 0.05) during muscle contraction, and localized Ca2+ transients were increased (>20%, P < 0.05) during the first minute after contraction. Chelation of EC Ca2+ abolished the dilatations in response to muscle contraction (1.1 ± 0.7 µm, P < 0.05). Inhibition of P1 purinergic receptors (with xanthine amine congener) did not alter the rate of onset of the dilatation (P > 0.05) but decreased its magnitude immediately post stimulation (7.1 ± 0.9 µm, P < 0.05) and during recovery. These findings demonstrate obligatory roles for endothelium and EC Ca2+ during metabolic dilatation in intact arterioles. Furthermore, they suggest that at least two separate pathways mediate the local response, one of which involves stimulation of endothelial P1 purinergic receptors via endogenous adenosine produced during muscle activity.
(Received 9 July 2003;
accepted after revision 19 December 2003;
first published online 23 December 2003)
Corresponding author I. H. Sarelius: Department Pharmacology and Physiology, University of Rochester Medical Center, Box 711, Rochester, NY 14642, USA. Email: ingrid_sarelius{at}urmc.rochester.edu
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